In-Plane Anisotropies of Polarized Raman Response and Electrical Conductivity in Layered Tin Selenide

The group IV-VI compound SnSe, with an orthorhombic lattice structure, has recently attracted particular interest due to its unexpectedly low thermal conductivity and high power factor, showing great promise for thermoelectric applications. SnSe displays intriguing anisotropic properties due to the puckered low-symmetry in-plane lattice structure. Low-dimensional materials have potential advantages in improving the efficiency of thermoelectric conversion, due to the increased power factor and decreased thermal conductivity. A complete study of the optical and electrical anisotropies of SnSe nanostructures is a necessary prerequisite in taking advantage of the material properties for high performance devices. Here, we synthesize the single crystal SnSe nanoplates (NPs) by chemical vapor deposition. The angular dependence of the polarized Raman spectra of SnSe NPs shows anomalous anisotropic light-mater interaction. The angle-resolved charge transport of the SnSe NPs expresses a strong anisotropic conductivity behavior. These studies elucidate the anisotropic interactions which will be of use for future ultrathin SnSe in electronic, thermoelectric and optoelectronic devices.Comment: 25 pages, 9 figures, 3 table

The ClpP protease homologue is required for the transmission traits and cell division of the pathogen Legionella pneumophila

<p>Abstract</p> <p>Background</p> <p><it>Legionella pneumophila</it>, the intracellular bacterial pathogen that causes Legionnaires' disease, exhibit characteristic transmission traits such as elevated stress tolerance, shortened length and virulence during the transition from the replication phase to the transmission phase. ClpP, the catalytic core of the Clp proteolytic complex, is widely involved in many cellular processes via the regulation of intracellular protein quality.</p> <p>Results</p> <p>In this study, we showed that ClpP was required for optimal growth of <it>L. pneumophila </it>at high temperatures and under several other stress conditions. We also observed that cells devoid of <it>clpP </it>exhibited cell elongation, incomplete cell division and compromised colony formation. Furthermore, we found that the <it>clpP</it>-deleted mutant was more resistant to sodium stress and failed to proliferate in the amoebae host <it>Acanthamoeba castellanii</it>.</p> <p>Conclusions</p> <p>The data present in this study illustrate that the ClpP protease homologue plays an important role in the expression of transmission traits and cell division of <it>L. pneumophila</it>, and further suggest a putative role of ClpP in virulence regulation.</p

Evaluation of installation timing of initial ground support for large-span tunnel in hard rock

In conventional drill and blast tunnelling, initial ground support is placed immediately after the current round is shot before excavation of the next round (i.e. one-round installation method). When tunnelling in hard rock, one-round installation of initial ground support conservatively ensures tunnel integrity, but meanwhile brings up other problems such as over-break at tunnel face, slow excavation rate and so forth. In this study, a large-span tunnel in Class III hard rock was monitored by a network of sensors to investigate tunnel internal forces in three construction scenarios where initial ground supports were placed in different timing and sequence: (1) initial ground support installed immediately after current round (2) support installed after two rounds (3) support installed after three consecutive rounds. The collected field measurements together with construction records were evaluated from three aspects: structural stability, constructability and cost-effectiveness. Results show that the installation of initial ground support after two rounds generally led to the most regular and minimum tunnel internal forces of the three construction scenarios, whilst it managed to minimize under & over-break and allow more space for construction convenience. In the meanwhile, this installation sequence significantly accelerated tunnel advance rate at lower material cost

IKKβ programs to turn on the GADD45α–MKK4–JNK apoptotic cascade specifically via p50 NF-κB in arsenite response

Cross talk between NF-κB and c-Jun N-terminal kinases (JNKs) has been implicated in the cell life and death decision under various stresses. Functional suppression of JNK activation by NF-κB has recently been proposed as a key cellular survival mechanism and contributes to cancer cells escaping from apoptosis. We provide a novel scenario of the proapoptotic role of IκB kinase β (IKKβ)–NF-κB, which can act as the activator of the JNK pathway through the induction of GADD45α for triggering MKK4/JNK activation, in response to the stimulation of arsenite, a cancer therapeutic reagent. This effect of IKKβ–NF-κB is dependent on p50 but not the p65/relA NF-κB subunit, which can increase the stability of GADD45α protein through suppressing its ubiquitination and proteasome-dependent degradation. IKKβ–NF-κB can therefore either activate or suppress the JNK cascade and consequently mediate pro- or antiapoptotic effects, depending on the manner of its induction. Furthermore, the NF-κB p50 subunit can exert a novel regulatory function on protein modification independent of the classical NF-κB transcriptional activity

(E)-N′-(4-Nitro­benzyl­idene)-4-(8-quinol­yloxy)butano­hydrazide

In the title compound, C20H18N4O4, conformation along the bond sequence linking the benzene and quinoline rings, which have a mean inter­planar dihedral angle of 2.7 (5)°, is trans–(+)gauche–trans–trans–(−)gauche–trans–trans. In the crystal structure, a pair of inter­molecular N—H⋯O hydrogen bonds links the mol­ecules into centrosymmetric cyclic R 2 2(8) dimers, which are aggregated via π–π inter­actions into parallel sheets [quinoline–benzene ring centroid separation = 3.6173 (16)–3.6511 (16) Å]. The sheets are further connected through weak C—H⋯O inter­actions, giving a supra­molecular two-dimensional network

Study of H2S Removal Capability from Simulated Biogas by Using Waste-Derived Adsorbent Materials

Funding: This work was part of the research activities carried out in the framework of the “European Biofuels Research Infrastructure for Sharing Knowledge 2 (BRISK2)” project under grant agreement 731101 (https://brisk2.eu/) and the European Commission is acknowledged for co-funding the work.Peer reviewedPublisher PD

Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation

Communication between the SR (sarcoplasmic reticulum, SR) and mitochondria is important for cell survival and apoptosis. The SR supplies Ca2+ directly to mitochondria via inositol 1,4,5-trisphosphate receptors (IP3Rs) at close contacts between the two organelles referred to as mitochondrion-associated ER membrane (MAM). Although it has been demonstrated that CaR (calcium sensing receptor) activation is involved in intracellular calcium overload during hypoxia/reoxygenation (H/Re), the role of CaR activation in the cardiomyocyte apoptotic pathway remains unclear. We postulated that CaR activation plays a role in the regulation of SR-mitochondrial inter-organelle Ca2+ signaling, causing apoptosis during H/Re. To investigate the above hypothesis, cultured cardiomyocytes were subjected to H/Re. We examined the distribution of IP3Rs in cardiomyocytes via immunofluorescence and Western blotting and found that type 3 IP3Rs were located in the SR. [Ca2+]i, [Ca2+]m and [Ca2+]SR were determined using Fluo-4, x-rhod-1 and Fluo 5N, respectively, and the mitochondrial membrane potential was detected with JC-1 during reoxygenation using laser confocal microscopy. We found that activation of CaR reduced [Ca2+]SR, increased [Ca2+]i and [Ca2+]m and decreased the mitochondrial membrane potential during reoxygenation. We found that the activation of CaR caused the cleavage of BAP31, thus generating the pro-apoptotic p20 fragment, which induced the release of cytochrome c from mitochondria and the translocation of bak/bax to mitochondria. Taken together, these results reveal that CaR activation causes Ca2+ release from the SR into the mitochondria through IP3Rs and induces cardiomyocyte apoptosis during hypoxia/reoxygenation